Three-dimensional images of coronary arteries after heart transplantation using electron-beam computed tomography data with volume rendering.
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Biomedical subjects
Publications and source records attributed to Y Kobayashi.
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The relative Lewis basicities of six Al(ORF)4- ions, Al[OC(CH3)(CF3)2]4-, Al(OC(CF3)3]4-, Al(OCPh(CF3)2]4-, Al[OC[4-C6H4(tBu)](CF3)2]4-, Al(OC(Cy)(CF3)2]4-, and Al(OCPh2(CF3)]4-, have been determined by measuring their relative coordinating abilities towards Li+ in dichloromethane. The relative Li- Lewis basicities of the Al(ORF)4- ions are linearly related to the aqueous pKa values of the corresponding parent HORF fluoroalcohols. The Lewis basicity of Al[OCH(CF3)2]4- could not be measured because two of these anions can coordinate to one Li+ cation. The structures of LiAl[OCH(CF3)2]4 and [1-Et-3-Me-1,3-C3H3N2][Li[Al[OCH(CF3)2)4]2] were determined.
It was found that the self-aggregation of IgA1 was closely connected with the glycoform of a mucin-type sugar chain on its hinge portion. In this report, normal human serum IgA1 was separated into two subfractions by a jacalin column. The elution condition, 25 mM galactose, used here was similar to that reported for the glycoprotein with a single mucin-type sugar chain per molecule. The IgA1 eluted under this condition was substantially the monomeric form. In contrast, the remaining IgA1 eluted from the column with 0. 8 M galactose was substantially the aggregated form. An analytical method for the microheterogeneity of the IgA1 hinge glycopeptide (HGP33) was developed to determine the difference between these IgA1 fractions by capillary electrophoresis (CE). Native HGP33 from both IgA1 fractions was separated into peaks 1-11, depending on their glycoforms. Because the sialic acid-rich component migrated slowly on CE, the 25 mM fraction was abundant in the sialic acid-rich components (peaks 7-11), but the 0.8 M fraction was abundant in the sialic acid-poor components (peaks 1-4). Comparison of the number of sugar chains per hinge peptide indicated that the 25 mM fraction was relatively well glycosylated. Thus, application of CE analysis to the HGP33 indicated that the monomeric IgA1 was composed of a relatively complete molecule with respect to the glycoform rather than the aggregated IgA1.
The relationship between the levels of serum cystatin C and the prognostic stages of IgA nephropathy was determined in a multicenter trial in Japan. The levels of serum cystatin C in patients with IgA nephropathy were measured using the Dade Behring N Latex Cystain C assay. In 1995, the Joint Committee of the Special Study Group on Progressive Glomerular Diseases, Ministry of Health and Welfare of Japan, and the Japanese Society of Nephropathy reported four prognostic stages. These are: good prognosis group (Group I), relatively good prognosis group (Group II), relatively poor prognosis group (Group III), and poor prognosis group (Group IV), for this disease. Three-hundred and six patients with IgA nephropathy and other glomerular diseases were examined. There were no significant changes in the levels of serum creatinine (Cr) or creatinine clearance (CCr) between Group I and Group II. The mean levels of serum cystatin C in Group II were significantly higher than those in Group I (P < 0.05). The mean levels of serum cystatin C in Group III or IV were significantly higher than those in Group I (P < 0.001, P < 0.005, respectively). These suggest that the measurement of serum cystatin C may predict the prognostic stages of patients with IgA nephropathy prior to renal biopsy.
We report treatment of a lesion with coronary stent underexpansion due to heavily calcified plaque. Conventional balloon angioplasty was attempted for in-stent restenosis, but the lesion was undilatable despite 25-atm inflation pressure. Intravascular ultrasound (IVUS) revealed stent underexpansion due to heavily calcified plaque. Rotational atherectomy was performed using a stepped burr approach, after which repeat IVUS revealed marked ablation of the stent-calcium complex. Adjunctive balloon angioplasty then easily resulted in full balloon and stent expansion, with an excellent angiographic and IVUS result. The patient's hospital course was uneventful.
Essential thrombocythemia (ET) is a clonal myeloproliferative disorder characterized by an elevation of platelets in peripheral blood and excessive proliferation of megakaryocytes in bone marrow. The pathological mechanisms for the elevation of megakaryocytes and platelets in ET remain unclear. To study the hypersensitivity of megakaryocyte progenitors to thrombopoietin (TPO), a 9-year-old girl, diagnosed with ET, underwent dose-response experiments with recombinant human TPO, using her bone marrow non-adherent mononuclear cells and CD34 positive cells. Spontaneous colony-forming unit-megakaryocytes (CFU-Meg) were observed in serum-deprived cultures of non-adherent mononuclear cells, whereas they disappeared in cultures of CD34 positive cells. The patient's CFU-Meg showed maximal growth at concentrations of TPO lower than those for normal children. Dose-response curves demonstrated a 50-80 fold increase in sensitivity of the patient's CFU-Meg to TPO. We observed hypersensitivity of megakaryocyte progenitors to TPO in a child with ET. Our results suggest that spontaneous CFU-Meg formation in patients with ET may be due to hypersensitivity to TPO.
We report five cases treated with brachytherapy through the internal mammary artery (IMA) for in-stent restenosis at the distal anastomosis (n = 3) and in the left anterior descending coronary artery beyond the distal anastomosis (n = 2). After angioplasty, catheter-based gamma radiation was performed. There was no delivery failure of the radiation system. All cases had angiographic success and no procedural or in-hospital complications.
BACKGROUND: Matrix metalloproteinase-7 (MMP-7) is a member of the MMP family and has a wide variety of substrate spectra. Ets domain transcription factors are reported to play an important role in carcinoma invasion and metastasis. The regulatory role of Ets-1 has been shown in several MMPs. We have hypothesized that MMP-7 and Ets-1 mRNA levels could be predictors of the development and invasion of lung cancer. METHODS: The study included 73 lung cancer cases. The mRNA levels were quantified by real-time reverse transcription-polymerase chain reaction (RT-PCR) using a LightCycler. RESULTS: No significant difference in MMP-7 and Ets-1 mRNA levels was found among gender, age, and pathological subtype. The MMP-7 mRNA levels were elevated in tumor tissues from stage II-IV lung cancer (1.629 +/- 2.267) compared to those from stage I lung cancer (0.762 +/- 1.463) (P = 0.0290). There was a tendency toward higher MMP-7 mRNA expression levels in tumors with lymph node metastasis (1.728 +/- 2.432) compared to those without lymph node metastasis (1.141 +/- 1.838) (P = 0.1076). Thus, MMP-7 mRNA levels may serve as a marker of higher stages in lung cancer. No significant difference in Ets-1 mRNA levels was found among clinical stages and T-status. The Ets-1 mRNA levels were elevated in tumors from N2 patients (7.512 +/- 13.306) compared to those from N0 patients (2.525 +/- 4.719) (P = 0.0209). Ets-1 mRNA levels showed a positive correlation with MMP-7 expression (P = 0.0042). CONCLUSIONS: Using the LightCycler RT-PCR assay, the determination of MMP-7 and Ets-1 mRNA levels might provide a potential marker for advanced lung cancer. However, further studies and a longer follow-up are needed to confirm the impact of MMP-7 in the biological behavior of the tumor.
Porcine edema disease (ED) is an enterotoxaemia in pigs after weaning, caused by Shiga toxin 2e (Stx2e) producing Escherichia coli. Recently in Japan, outbreaks of ED are re-emerging in pig production. In this study we constructed a mutant that retained immunogenicity but lost Vero cell cytotoxicity, which produced genetically modified toxin (Stx2e*) by replacing glutamate with glutamine at position 167 and arginine with leucine at position 170 of the A subunit. The stx(2e)* gene was replaced with the stx(2e)gene of the wild type virulent strain by homologous recombination. As the parent wild strain was pathogenic to pigs but the mutant was not, the mutant named as YT106 was given to the pigs to examine its protective immunity against ED. All 20 pigs vaccinated with YT106 survived, but only eight of the 20 non-vaccinated pigs survived after the challenge with a wild strain. Also, the eight pigs that survived had decreased rates of gain relative to those of the controls. Blood IgG and intestinal IgA titres increased 3.3 and 1.6 times more than the control, respectively, showing that YT106 might be a good candidate of a live attenuated vaccine strain to protect against ED.
Among 55 Butyrivibrio fibrisolvens strains five ribotypes of B. fibrisolvens were described on the basis of RFLP profiles of 16S rDNA regions obtained with restriction endonuclease HaeIII. In the phylogenetic tree, these ribotypes were located in the XIVa cluster of Gram-positive bacteria. Phenotypic differences of selected ribotype groups became the basis for further reclassification of B. fibrisolvens.
OBJECTIVES: Concordant cardiac xenografts are known for delayed vascular rejection. Therapy combining with FK506 and cobra venom factor prolongs graft survival. The proposed underlying mechanism holds that cytoprotective proteins such as Bcl-2 play a role here. We studied the effects of gene transfection of human-bcl-2 on graft survival and coronary artery lesions in concordant cardiac xenografts, and discuss the role of cytoprotective genes in vascular xenograft rejection. METHODS: Golden-Syrian-hamster hearts were heterotopically transplanted into Lewis rats given FK506 (1 mg/kg daily) and cobra venom factor (0.2 mg/kg; day 0 and 1) intramuscularly. They were divided into 2 groups--grafts transfected vector with the human-bcl-2 gene (Group-B(+)) and vector without the gene (Group-B(-)) using the HVJ liposome method; 4 or 5 grafts from each group were explanted 1, 2, 3, or 4 weeks and more than 1 month after transplantation and evaluated by H-E, Elastic-Van-Gieson and immunohistochemical staining of Bcl-2. Coronary arterial lesions were examined using a scoring method. RESULTS: Bcl-2 expression in endothelial cells in Group-B(+) was confirmed within 2 weeks after transplantation but not thereafter. The coronary score in Group-B(+) was significantly lower than that in Group-B(-) within 2 weeks after transplantation but not thereafter. CONCLUSIONS: In this hamster-to-rat cardiac xenograft model, the bcl-2 gene was successfully transfected to the coronary endothelium and lasted 2 weeks. During Bcl-2 expression, coronary vascular lesions were suppressed more than in the untransfected group.
The purpose of this study was to investigate the toxicity and the efficacy of re-treatment with rituximab, a chimeric mouse human anti-CD20 monoclonal antibody, in relapsed patients with indolent B-cell non-Hodgkin's lymphoma (NHL) who responded to rituximab in the previous phase I or phase II study. Thirteen patients with relapsed B-cell NHL, each of whom was confirmed to have Revised European-American Lymphoma Classification type II, 1-6 histology (indolent B-NHL), enrolled in this re-treatment study. All were re-treated with rituximab at 375 mg/m2 weekly for 4 consecutive weeks. Rituximab re-treatment was well tolerated with no grade 3/4 nonhematological toxicities, similar to that of the initial treatment. No patients developed detectable human anti-chimeric antibody. Partial responses were observed in 5 of 13 patients (38%; 95% confidence interval [CI], 14% to 68%); 6 patients showed stable disease and 2 showed progressive disease. Overall survival rate was 93% at 19 months of median follow-up after rituximab re-treatment. Median progression-free survival (PFS) after the re-treatment was 5.1 months (95% CI, 4.1 to 5.6 months), and the median PFS after the initial treatment was 8.2 months (95%CI, 5.9 to 11.3 months). Although rituximab re-treatment induced prolonged depletion of normal peripheral blood B cells in all patients, no significant decrease in serum immunoglobulin or complement level was observed. In conclusion, rituximab re-treatment was well tolerated, and it may produce a prolonged PFS in some patients with indolent B-cell NHL who showed initial response to rituximab.
Idiopathic hypereosinophilic syndrome (HES) is a heterogeneous group of disorders with the common features of prolonged eosinophilia of underdetermined cause and multiple organ system dysfunction. Focal eosinophilic myositis is an uncommon manifestation of HES. We report a case of focal eosinophilic myositis with tender muscle swelling followed by proximal weakness, but without non-systemic symptoms and muscle trophism in the lower limbs. Muscle biopsy specimen showed acute myositis with eosinophil infiltration. Electromyographic features were typical of myositis. The clinical and biochemical response to corticosteroids was excellent, and a relapse that occurred because the steroid dose was not lowered, responded well.
An efficient system to produce saikosaponins (saikosaponin-a and -d) in Bupleurum falcatum adventitious root fragments combined with signal transducers was developed. The roots are heterogeneous in terms of size and shape and sometimes form aggregates during cultivation. When the roots were cut to lengths of about 5 mm using a scalpel and cultivated, the root fragments did not form the aggregates, and root growth and saikosaponin production were not inhibited. After screening various signal transducers, it was clear that methyl jasmonate (MeJA) markedly promoted saikosaponin production. By comparing the effect of MeJA and related substances on saikosaponin production, we conclude that both the pentenyl and carboxylmethyl group of MeJA play an important role in the promotion of saikosaponin production. Addition of both 100 microM MeJA and 20 mM CaCl2 to the medium stimulated the content of saikosaponin in the root, with levels reaching 31.7 mg/g-dry root for 15 days of cultivation. A large amount of root fragments were prepared using a blender and cultivated (23 g-dry root/l) with 400 microM MeJA and 20 mM CaCl2, resulting in a high concentration of saikosaponins (747.3 mg/l).
Ligamentous calcification of the cervical spine has been reported in the yellow ligament, anterior and posterior longitudinal ligaments and interspinous ligament. Calcification in the upper cervical spine is rare, although some cases with calcification of the transverse ligament of the atlas have been reported. Two patients with calcification of the alar ligament with an unusual clinical presentation and course are described. Examination by tomography and computed tomography (CT) showed calcification of the alar ligament and the transverse ligament of the atlas. CT documented decreased calcification as symptoms resolved. There may be a role for CT in the search for calcifications in the upper cervical spine in patients presenting with neck pain and pharyngodynia if radiographs are normal.
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Thrombopoietin (TPO) plays a critical role not only in proliferation and differentiation of megakaryocytes but also in erythroid differentiation. We have investigated whether the different pathway of mitogen-activated protein kinase (MAPK) after TPO stimulation may discriminate megakaryocyte and erythroid differentiation. In this study, we have used human CD34+ hematopoietic progenitor cells (HPCs) from cord blood (CB) in serum-free liquid culture supplemented with TPO, to compare the respective effects of specific inhibitors of MAPK kinase (MEK) (PD98059) and p38 MAP kinase (p38) (SB203580) on megakaryocyte and erythroid development. PD98059, but not SB203580, significantly suppressed TPO-induced megakaryocyte differentiation when examined by the expression of CD41 and polyploidy assay. In the presence of SB203580, CD34+/CD36+ erythroid progenitors clearly decreased, whereas they increased when cultured with PD98059. These results indicate that activation of extracellular-signal-regulated kinase (ERK) is required for TPO-induced megakaryocyte differentiation and that p38 is required for TPO-induced erythroid differentiation.
The imaging features of primary pericardial mesothelioma have rarely been described. Herein we present a case report of its diagnostic-pathologic features. Chest computed tomography (CT) revealed an irregularly enhanced mass occupying the entire pericardial space and surrounding the superior vena cava. At autopsy, the tumor was found to fill the pericardial space completely, and to extend to the superior vena cava through the superior pericardial sinus. The CT features of the tumor were correlated well with those revealed at autopsy, and provided satisfactory information regarding the presence and the extension of the tumor.